Significance Characterized by a growing number of opportunities infections and diseases, AIDS develops as a result of viral-induced immunosuppression in a host infected with the Human Immunodeficiency Virus (HIV). Cells infected by HIV consist of mainly T lymphocytes and macrophages, which are largely responsible for maintaining cell-mediated immunity. Little has been done, however, to investigate the extent of infection in other types of immune cells, such as polymorphonuclear neutrophils (PMN). Objectives Rhesus monkeys infected with simian immunodeficiency virus (SIV) have been an excellent animal model for the study of HIV infection and human AIDS. The present study was undertaken to determine whether SIV can infect monkey-derived PMN. PMN pathogenesis was studied through an in vitro infection of healthy rhesus macaque PMN with the molecular clone SIVmac239. The intracellular alterations after the infection and the PMN cell viability associated with the programmed cell death (apoptosis) were also studied. Results Using the polymerase chain reaction (PCR) technique, we detected the presence of SIVmac239 DNA in rhesus macaque-derived PMN after 24 hrs of in vitro incubation of the cells with SIVmac239. Infection by SIVmac239 also down-regulates the expression of the bcl-2 apoptosis-blocking gene in the infected PMN. These SIVmac239 induced PMN intracellular alterations were correlated with an accelerated decrease in PMN viability over a period of 120 hrs compared to non-infected PMN. Evidence of chromatin condensation characteristic of programmed cell death (apoptosis) was also observed in SIVmac239-infected PMN. The results of this study provide a mechanism for the reduced chemotaxis/phagocytosis activities of PMN of SIVmac239-infected macaques and suggest that PMN is one of the target cells for SIVmac239 infection. Future Directions Additional studies examining other PMN cell parameters in the presence of SIVmac239 infections are currently under investigation. KEY WORDS rhesus monkeys, SIVmac239, PMN, apoptosis, AIDS FUNDING NIH Grant DA05901